![]() have found that the transcription factor NF-κB occupies a significant role in the pathogenesis of RA. A study suggests that canonical Wnt and NF-κB signaling pathways take part in the hypernociception and inflammatory response in the temporomandibular joint synovial membrane during the development of RA in rats. The nuclear factor-κB (NF-κB) family of transcription factors is activated via canonical and non-canonical signaling pathways, which own differences in both signaling elements and biological functions. What is more, RIPK1 knockdown can improve the inflammatory response in collagen‑induced arthritis through inhibition of necroptosis. The other study finds that RIPK1-VDAC1 binding is a possible target to treat cardiac impairment in RA. The receptor-interacting serine/threonine protein kinase 1 (RIPK1) can lead to two apparent forms of cell death, including RIPK3-mediated necroptosis or caspase 8 (Casp8)-mediated apoptosis. In addition, a study observed that miR-338-5p could regulate RA pathogenesis by directly binding to its target gene. MiR-411 is regarded as a tumor suppressor in renal cell cancer, while performing as an oncogene in osteosarcoma. At present, many types of miRNAs have been reported to be closely connected with the occurrence and development of tumors. MicroRNAs (miRNAs) are single-stranded small non-coding RNAs with a length of 18–25 nucleotides. However, the optimal treatment strategy is uncertain, so it is urgent to seek new therapeutic targets to improve the prognosis of RA. Traditionally, the therapeutic method of RA is drug therapy, including non-steroidal anti-inflammatory drugs, glucocorticoids, and disease-modifying antirheumatic drugs. A study has been implemented on the mechanism of RA which revealed that the occurrence of RA is due to a complex interaction of environmental exposures and susceptible genetic background. RA is a disease featured by chronic inflammation of the synovium, synovial hyperplasia, pannus formation, and erosive lesions of the cartilage and bone tissue and owns a lower general prevalence in China. Rheumatoid arthritis (RA) is a systematic autoimmune illness, mainly leading to chronic polyarticular inflammation and joint injury of patients. This study suggests that up-regulated miR-411 or down-regulated RIPK1 promoted apoptosis and inhibited proliferation of synoviocytes of RA mice, which may be related to the inhibition of NF-κB activation. Up-regulation of miR-411 or down-regulation of RIPK1 had a certain inhibitory effect on RA. Overexpressed miR-411 or silencing RIPK1 inhibited the proliferation and promoted apoptosis of synoviocytes of RA mice. si-RIPK1 or miR-411 mimics promoted cell apoptosis and strained inflammation in synovial tissues of mice with RA. MiR-411 had a targeted relationship with RIPK1. Additionally, it was found that si-RIPK1 decreased NF-κB expression, and miR-411 mimics decreased both RIPK1 and NF-κB. Poorly expressed miR-411, and highly expressed NF-κB and RIPK1 existed in synovial tissue and synoviocytes of RA. The expression of miR-411, RIPK1 and NF-κB in synovial tissues and synoviocytes of RA mice was detected by RT-qPCR and Western blot analysis. Proliferation and apoptosis of synoviocytes were detected upon treatment with overexpressed miR-411 and silenced RIPK1. ![]() Synoviocytes were grouped as in animal experiments. ![]() The mice were injected with miR-411 mimics, si-RIPK1 or miR-411 mimics + oe-RIPK1 to figure out their roles in cell apoptosis and inflammation of synovial tissues. The collagen-induced arthritis model mice were induced via collagen type II and Freund’s adjuvant. Due to the unknown pathogenesis, this study was to investigate the effect of microRNA (miR)-411 on apoptosis and joint function of synoviocytes in RA mice via RIPK1-mediated NF-κB signaling pathway. ![]() Rheumatoid arthritis (RA) is a chronic and inflammatory synovitis systemic disease.
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